• 제목/요약/키워드: autonomous cell activation

검색결과 9건 처리시간 0.024초

A Reinforcement Learning Framework for Autonomous Cell Activation and Customized Energy-Efficient Resource Allocation in C-RANs

  • Sun, Guolin;Boateng, Gordon Owusu;Huang, Hu;Jiang, Wei
    • KSII Transactions on Internet and Information Systems (TIIS)
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    • 제13권8호
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    • pp.3821-3841
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    • 2019
  • Cloud radio access networks (C-RANs) have been regarded in recent times as a promising concept in future 5G technologies where all DSP processors are moved into a central base band unit (BBU) pool in the cloud, and distributed remote radio heads (RRHs) compress and forward received radio signals from mobile users to the BBUs through radio links. In such dynamic environment, automatic decision-making approaches, such as artificial intelligence based deep reinforcement learning (DRL), become imperative in designing new solutions. In this paper, we propose a generic framework of autonomous cell activation and customized physical resource allocation schemes for energy consumption and QoS optimization in wireless networks. We formulate the problem as fractional power control with bandwidth adaptation and full power control and bandwidth allocation models and set up a Q-learning model to satisfy the QoS requirements of users and to achieve low energy consumption with the minimum number of active RRHs under varying traffic demand and network densities. Extensive simulations are conducted to show the effectiveness of our proposed solution compared to existing schemes.

Cell Cycle-Dependent Activity Change Of $Ca^{2+}/$Calmodulin-Dependent Protein Kinase II In NIH 3T3 Cells

  • Kim, Dae-Sup;Suh, Kyong-Hoon
    • BMB Reports
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    • 제34권3호
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    • pp.212-218
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    • 2001
  • Although the blockage of a cell cycle by specific inhibitors of $Ca^{2+}/$calmodulin-dependent protein kinase II (CaMK-II) is well known, the activity profile of CaMK-II during the cell cycle in the absence of any direct effectors of the enzyme is unclear. The activity of native CaMK-II in NIH 3T3 cells was examined by the use of cell cycle-specific arresting and synchronizing methods. The total catalytic activity of CaMK-II in arrested cells was decreased about 30% in the M phase, whereas the $Ca^{2+}$-independent autonomous activity increased about 1.5-fold in the M phase and decreased about 50% at the G1/S transition. The in vivo phosphorylation level of CaMK-II was lowest at G1/S and highest in M. The CaMK-II protein level was unchanged during the cell cycle. When the cells were synchronized, the autonomous activity was increased only in M. These results indicate that the physiologically relevant portion of CaMK-II is activated only in M, and that the net activation of CaMK-II is required in mitosis.

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Application of Adaptive Neuro-Fuzzy Inference System for Interference Management in Heterogeneous Network

  • Palanisamy, Padmaloshani;Sivaraj, Nirmala
    • ETRI Journal
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    • 제40권3호
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    • pp.318-329
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    • 2018
  • Femtocell (FC) technology envisaged as a cost-effective approach to attain better indoor coverage of mobile voice and data service. Deployment of FCs over macrocell forms a heterogeneous network. In urban areas, the key factor limits the successful deployment of FCs is inter-cell interference (ICI), which severely affects the performance of victim users. Autonomous FC transmission power setting is one straightforward way for coordinating ICI in the downlink. Application of intelligent control using soft computing techniques has not yet explored well for wireless networks. In this work, autonomous FC transmission power setting strategy using Adaptive Neuro Fuzzy Inference System is proposed. The main advantage of the proposed method is zero signaling overhead, reduced computational complexity and bare minimum delay in performing power setting of FC base station because only the periodic channel measurement reports fed back by the user equipment are needed. System level simulation results validate the effectiveness of the proposed method by providing much better throughput, even under high interference activation scenario and cell edge users can be prevented from going outage.

지속적으로 발현되는 융모성 성선자극호르몬 수용체의 기능 (Function of Constitutively Activating Lutropin/Choriogonadotropin Receptor)

  • Min, K. S.
    • 한국가축번식학회지
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    • 제24권1호
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    • pp.41-47
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    • 2000
  • 성선자극호르몬 수용체 (LH/CGR)는 7번 막을 통과하는 수용체의 일종이다. LH/CGR의 유전자 돌연변이 질환은 남성에 있어서 이들 수용체가 조기에 발현되어 조기 성숙의 원인이 된다. 이러한 수용체의 기능을 분석하기 위하여 556번째의 아미노산 (D)을 Y로 치환한 돌연변이 수용체 (D556Y)를 만들었다. 이러한 돌연변이 수용체를 동물세포에 발현시켜 cAMP의 분석결과 Ligand (호르몬)가 없어도 지속적으로 정보전달을 세포내부로 보내 cAMP 발현을 현저히 증가시켰다. 따라서 남성의 조기성숙과 관련된 질환은 지속적으로 발현하는 LH /CGR에 의한 원인 때문일 것이다.

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CROX (Cluster Regulation of RUNX) as a Potential Novel Therapeutic Approach

  • Kamikubo, Yasuhiko
    • Molecules and Cells
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    • 제43권2호
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    • pp.198-202
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    • 2020
  • Comprehensive inhibition of RUNX1, RUNX2, and RUNX3 led to marked cell suppression compared with inhibition of RUNX1 alone, clarifying that the RUNX family members are important for proliferation and maintenance of diverse cancers, and "cluster regulation of RUNX (CROX)" is a very effective strategy to suppress cancer cells. Recent studies reported by us and other groups suggested that wild-type RUNX1 is needed for survival and proliferation of certain types of leukemia, lung cancer, gastric cancer, etc. and for their one of metastatic target sites such as born marrow endothelial niche, suggesting that RUNX1 often functions oncogenic manners in cancer cells. In this review, we describe the significance and paradoxical requirement of RUNX1 tumor suppressor in leukemia and even solid cancers based on recent our findings such as "genetic compensation of RUNX family transcription factors (the compensation mechanism for the total level of RUNX family protein expression)", "RUNX1 inhibition-induced inhibitory effects on leukemia cells and on solid cancers through p53 activation", and "autonomous feedback loop of RUNX1-p53-CBFB in acute myeloid leukemia cells". Taken together, these findings identify a crucial role for the RUNX cluster in the maintenance and progression of cancers and suggest that modulation of the RUNX cluster using the pyrrole-imidazole polyamide gene-switch technology is a potential novel therapeutic approach to control cancers.

인공 면역계를 기반으로 하는 적응형 침입탐지 알고리즘 (Adaptive Intrusion Detection Algorithm based on Artificial Immune System)

  • 심귀보;양재원
    • 한국지능시스템학회논문지
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    • 제13권2호
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    • pp.169-174
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    • 2003
  • 인터넷 보급의 확산과 전자상거래의 활성화 그리고 유ㆍ무선 인터넷의 보급에 따른 악의적인 사이버 공격의 시도가 점점 증가하고 있다. 이로 인해 점차 더 많은 문제가 야기될 것으로 예상된다. 현재 일반적인 인터넷상의 시스템은 악의적인 공격에 적절하게 대응해오지 못하고 있으며, 다른 범용의 시스템들도 기존의 백신 프로그램에 의존하며 그 공격에 대응해오고 있다. 따라서 새로운 침입에 대하여는 대처하기 힘든 단점을 가지고 있다. 본 논문에서는 생체 자율분산시스템의 일부분인 T세포의 positive selection과 negative selection을 이용한 자기/비자기 인식 알고리즘을 제안한다 제안한 알고리즘은 네트워크 환경에서 침입탐지 시스템에 적용하여 기존에 알려진 침입뿐만 아니라 새로운 침입에 대해서도 대처할 수 있다.

생체 면역계를 이용한 네트워크 침입탐지 시스템 (Intrusion Detection System of Network Based on Biological Immune System)

  • 심귀보;양재원;이동욱;서동일;최양서
    • 한국지능시스템학회논문지
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    • 제12권5호
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    • pp.411-416
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    • 2002
  • 최근 인터넷의 확산과 전자상거래의 활성화 그리고, 유ㆍ무선 인터넷의 보급과 더불어 악의적인 사이버 공격의 시도와 성공이 급속하게 증가하고 있다. 이것은 점차 더 많은 문제를 야기할 것으로 예상된다. 현재 일반적인 인터넷상의 시스템은 악의적인 공격에 적절하게 대응하지 못하고 있으며, 다른 범용의 시스템들도 기존의 백신 프로그램에 의존하며 그 공격에 대응해오고 있다. 따라서 새로운 침입에 대하여는 대처하기 힘든 단점을 가지고 있다. 본 논문에서는 생체 자율분산시스템의 일부분인 T세포의 positive selection과 negative selection을 이용한 자기/비자기 인식 알고리즘을 제안한다 제안한 알고리즘은 네트워크 환경에서 침입탐지 시스템에 적용하여 기존에 알려진 침입뿐만 아니라 새로운 침입에 대해서도 대처할 수 있다.

Mutations of Constitutive Activation and Mutations That Impair Signal Transduction Modulate the Agonist-stimulated Internalization of the Lutropin/choriogonadotropin Receptor

  • Park, J.J.;Kim, M.S.;Lee, Y.Y.;H.Y. Kang;Y.M. Chang;Yoon, J.T.;K.S. Min
    • 한국발생생물학회:학술대회논문집
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    • 한국발생생물학회 2003년도 제3회 국제심포지움 및 학술대회
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    • pp.83-83
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    • 2003
  • The lutropin/choriogonadotropin receptor (LHR) is a member of the rhodopsin-like subfamily of G protein coupled receptor (GPCRs), that has been shown to mediate the internalization of its two naturally occurring agonist, lutropin and choriogonadotropin (CG). The clustered agonist-receptor complex is internalized by a dynamin-dependent pathway and traverses the endosomal compartment without agonist dissociation Dissociation of the agonist-receptor complex occurs in the lysosomes, where both the agonist and receptor are degrade. Recently, constitutively activating mutations of the receptor have been identified that are associated with familial male-precocious puberty (FMPP). A FMPP is a form of sexual precocious puberty in boys in which testosterone levels are elevated independent of changes in luteinizing hormone-releasing hormone and serum luteinizing hormone levels, We have now analyzed two naturally occurring, constitutively active mutants of the human LHR. These mutations were introduced into the rat LHR (rLHR) and are designated L435R and D556Y. Cells expressing rLHR-D556Y bind human choriogonadotropin (hCG) with normal affinity, exhibit a 25-fold increase in basal cAMP and respond to hCG with a normal increase in cAMP accumulation. Cells expressing rLHR-L435R also bind hCG with normal affinity, exhibit a 47-fold increase in basal cAMP, and do not respond to hCG with a further increase in cAMP accumulation. This mutation enhances the internalization of the free and agonist-occupied receptors ~2- and ~17- fold, respectively We conclude that the state of activation of the rLHR can modulate its basal and/or agonist-stimulated internalization. Since the internalization of hCG is involved in the termination of hCG actions, we suggest that the lack of responsiveness detected in cells expressing rLHR-L435R is due to the fast rate of internalization of the bound hCG. The finding that membranes expressing rLHR-L435R respond to hCG with an increase in adenylyl cyclase activity supports this suggestion. Autonomous Leydig cell activity in FMPP is caused by a constitutively activating LH/CGR.

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p66Shc in sheep preimplantation embryos: Expression and regulation of oxidative stress through the manganese superoxide dismutase-reactive oxygen species metabolic pathway

  • Tong Zhang;Jiaxin Zhang;Ruilan Li
    • Animal Bioscience
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    • 제36권7호
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    • pp.1022-1033
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    • 2023
  • Objective: p66Shc, a 66 kDa protein isoform encoded by the proto-oncogene SHC, is an essential intracellular redox homeostasis regulatory enzyme that is involved in the regulation of cellular oxidative stress, apoptosis induction and the occurrence of multiple age-related diseases. This study investigated the expression profile and functional characteristics of p66Shc during preimplantation embryo development in sheep. Methods: The expression pattern of p66Shc during preimplantation embryo development in sheep at the mRNA and protein levels were studied by quantitative real-time polymerase chain reaction (RT-qPCR) and immunofluorescence staining. The effect of p66Shc knockdown on the developmental potential were evaluated by cleavage rate, morula rate and blastocyst rate. The effect of p66Shc deficiency on reactive oxygen species (ROS) production, DNA oxidative damage and the expression of antioxidant enzymes (e.g., catalase and manganese superoxide dismutase [MnSOD]) were also investigated by immunofluorescence staining. Results: Our results showed that p66Shc mRNA and protein were expressed in all stages of sheep early embryos and that p66Shc mRNA was significantly downregulated in the 4-to 8-cell stage (p<0.05) and significantly upregulated in the morula and blastocyst stages after embryonic genome activation (EGA) (p<0.05). Immunofluorescence staining showed that the p66Shc protein was mainly located in the peripheral region of the blastomere cytoplasm at different stages of preimplantation embryonic development. Notably, serine (Ser36)-phosphorylated p66Shc localized only in the cytoplasm during the 2- to 8-cell stage prior to EGA, while phosphorylated (Ser36) p66Shc localized not only in the cytoplasm but also predominantly in the nucleus after EGA. RNAi-mediated silencing of p66Shc via microinjection of p66Shc siRNA into sheep zygotes resulted in significant decreases in p66Shc mRNA and protein levels (p<0.05). Knockdown of p66Shc resulted in significant declines in the levels of intracellular ROS (p<0.05) and the DNA damage marker 8-hydroxy2'-deoxyguanosine (p<0.05), markedly increased MnSOD levels (p<0.05) and resulted in a tendency to develop to the morula stage. Conclusion: These results indicate that p66Shc is involved in the metabolic regulation of ROS production and DNA oxidative damage during sheep early embryonic development.